Archives of Medical Science最新文献

Introduction: Type 2 diabetes (T2D) and mild cognitive impairment (MCI) are interrelated conditions that significantly impair quality of life. This study aimed to identify a feasible biomarker for assessing T2D-MCI risk and to evaluate a potential therapeutic strategy.

Material and methods: We integrated data from the National Health and Nutrition Examination Survey (NHANES) with Mendelian randomization (MR) to investigate genetic causal relationships between T2D, MCI, and their shared biomarkers. Transcriptomic analysis identified T2D-associated genes. Clinical trials evaluated the short-term effects of modified fasting therapy (MFT) on glucose regulation and cognitive function. Cellular assays and patient samples were used to validate the regulatory roles of key genes in biochemical markers and downstream signaling pathways.

Results: Among 6,356 T2D and 1,138 MCI subjects, vitamin D, high-density lipoprotein cholesterol (HDL-C), globulin, and creatinine were associated with both conditions. MR analysis showed that higher HDL-C levels reduced T2D risk (0.9059, 95% CI: 0.8666-0.9470) but increased MCI risk (OR = 1.0482, 95% CI: 1.0216-1.0755). Nuclear factor I A (NFIA) was identified as a key HDL-C regulator. In a clinical cohort (17 T2D patients and 23 controls), MFT reduced body mass index fasting glucose and HDL-C, increased NFIA expression, and improved Montreal Cognitive Assessment scores, especially in T2D-MCI patients. HDL-C rebounded at 6 months. In vitro, NFIA overexpression increased intracellular HDL-C and suppressed NF-κB signaling, while NFIA knockdown reduced APOA1 and APOE.

Conclusions: HDL-C has divergent genetic effects on T2D and MCI. NFIA modulates HDL-C and NF-κB activity, supporting metabolic and cognitive improvements. Targeting NFIA through MFT may represent a promising strategy for T2D-MCI prevention and treatment.

Introduction: The chronic gynecological condition endometriosis affects about 10 percent of reproductive aged women and imposes a heavy physical and psychological burden. The impact of pain and infertility is well documented, but the link between endometriosis and mental health (depressive and anxiety), in particular, is not well studied. In this systematic review and meta-analysis, we synthesize evidence on the association between endometriosis and mental health outcomes, specifically anxiety and depression.Methods: PubMed, Cochrane Library and Google Scholar were searched comprehensively to identify studies that have reported the association of endometriosis and mental health outcomes. Nine studies were included after applying predefined inclusion and exclusion criteria from 1,632 articles screened. The Newcastle-Ottawa Scale (NOS) was used to assess study quality and random effects meta-analyses were performed using R. Relative risk (RR) values for anxiety and depression among women with endometriosis were pooled as the primary outcomes.

Results: The meta-analysis revealed a significant association between endometriosis and anxiety (pooled RR = 2.82; 95% CI: 1.69-4.68, p < 0.001) and depression (pooled RR = 2.93; 95% CI: 1.63-5.25, p < 0.001). Substantial heterogeneity was observed in both analyses (I ² = 100%), reflecting variability in study designs and populations. Funnel plots showed moderate asymmetry, suggesting potential publication bias. Statistical heterogeneity was further quantified with τ² values of 0.6032 for anxiety and 0.794 for depression, indicating considerable between-study variability. These findings underscore the heightened mental health burden in women with endometriosis.

Conclusions: Endometriosis patients are more likely to develop anxiety and depressive symptoms due to pain and diagnostic evaluation and related psychosocial factors. This study stresses the importance of integrated care, which involves screening and treatment for mental health problems in addition to conventional medical care. Future work should aim to reduce heterogeneity and examine potential pathways through which these relationships exist in order to develop specific prevention strategies.

Introduction: Diabetes mellitus (DM) is associated with increased mortality in hospitalized adults. However, data regarding the impact of DM on long-term mortality after discharge in very old patients are scarce. This prospective study assessed 3-year post-discharge mortality and its predictive factors in older patients, focusing on possible differences between patients with and without DM.

Material and methods: Medical history, chronic medication use, clinical and laboratory characteristics, Charlson Comorbidity Index (CCI), 5-item Fried Frailty Score (FFS), Clinical Frailty Scale (CFS), Barthel Index (BI), and Katz Index were recorded on admission.

Results: A total of 815 older adults (46.0% males) with a median age of 83.0 years (IQR: 77.0-88.0) were included in the study. The 3-year mortality rate was 54.9% in patients with DM (n = 368) and 60.2% in patients without DM (n = 447, p = 0.13 between groups). In multivariate logistic analysis, nursing home residency, higher CCI, higher CFS, higher FFS, lower BI, the total number of days of hospitalization in the past year, and hospital-acquired infections were independently associated with the 3-year mortality in both groups. In individuals with DM, lower body mass index (BMI) and elevated urine albumin-to-creatinine ratio (UACR) were identified as additional independent predictors of 3-year mortality.

Conclusions: A high post-discharge mortality rate was observed in very old patients. DM was not identified as an independent factor of post-discharge mortality. Assessment of frailty and disability in very old patients is important for predicting long-term post-discharge mortality. Additionally, in patients with DM, evaluating BMI and UACR may aid in better prediction of 3-year mortality.

Introduction: Lipoprotein (a) (Lp(a)) is a largely genetically determined (70-90%) independent risk factor for cardiovascular disease (CVD). However, clinicians often encounter adults/elder adults with elevated Lp(a), who are otherwise healthy and asymptomatic for atherosclerosis. We aimed to identify additional risk factors and conditions, apart from elevated Lp(a), which lead to atherosclerosis progression and CVD, and whether any protective factors mitigate Lp(a)-related risk.

Material and methods: In the STAR (Specialist Care Patients) Lp(a) study, we prospectively enrolled 2,594 consecutive patients aged over 50 years, who had elevated Lp(a), referred to two outpatient cardiology clinics. These patients were either healthy, or had established CVD or three or more cardiovascular risk factors. Lp(a) concentration was measured by enzyme-linked immunosorbent assay.

Results: Among adults > 50 years with Lp(a) ≥ 30 mg/dl (75 nmol/l) (mean Lp(a), 65.4 vs. 72.7 mg/dl, p = 0.118), healthy individuals and patients differed significantly in mean age (62.8 vs. 69.6 years, p < 0.001), body mass index (BMI) and prevalence of overweight/ obesity (16.0% vs. 32.7%, p = 0.001), mean hsCRP (2.12 vs. 2.35 mg/l, p = 0.007), dyslipidemia, mean glucose and HbA_1c levels (5.44% vs. 5.86%, p < 0.001), and coronary artery calcium (CAC) scores (43.1 vs. 339.9, p < 0.001). In multivariable analysis, the independent predictors of increased CAC in healthy individuals were gender and non-HDL-C, while in patients, the independent predictors were non-HDL-C and age. Correlation analysis showed that in healthy individuals, CAC correlated with gender and non-HDL-C, while in patients, CAC correlated with age, gender, non-HDL-C, HbA_1c, and Lp(a). Comparing sub-groups with Lp(a) > 50 mg/dl (125 nmol/l) (mean age: 62.3 vs. 69.2 years, p < 0.001; female: 77.8% vs. 68.5%, p = 0.021; mean Lp(a) : 87.8 vs. 88.8 mg/dl, p = 0.838), the independent predictors of CAC in healthy individuals were elevated hsCRP and gender, whereas in patients, they were age and Lp(a). Correlation analysis confirmed that Lp(a) was significantly associated with CAC in patients only, and LDL-C and hsCRP correlated with CAC in patients only.

Conclusions: In adults > 50 years with elevated Lp(a), Lp(a) - related risk of atherosclerosis progression can be substantially mitigated by addressing modifiable CVD risk factors, such as obesity, diabetes, inflammation, and dyslipidemia, preferably by early preventive measures. In our study cohort, Lp(a) was independently associated with atherosclerosis progression in the patient group only.